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C-type lectin receptors (CLR)
for fungal infections
lectin= carbohydrate binding protein
NOD-like receptors (NLR)
peptidoglycan fragments from bacteria
RIG-I-like receptors (RLRs)
viral RNA in cytoplasm
IL-2
from activated T-cells (TCR binding) or activated dendritic cells (PRR binding)
stimulates proliferation of activated T cells & increases NK/ CD8 killing capacity
IL-4
from dendritic cells & from Th2 cells
Th2 helper cell induction & cross-inhibition to block Th1 & Th17 differentiation
IL-6
from activated macrophages
fat & muscle metabolism (UCP), endogenous pyrogen → raises temperature
acute phase protein production → C-reactive protein & mannose binding lectin + other complement components
alone: T follicular helper cell induction
w TGF beta: Th17
IL-10
anti-inflammatory produced by macrophages after engulfing apoptotic neutrophils
EBV→ vIL-10 which is anti-inflammatory mimic
Treg produces
IL-12
From macrophages to recruit & activate NK cells (IFN-gamma then causes M1 polarisation)
from dendritic cells for Th1 specification
Th1 cells
Induced by IL-12 release from dendritic cells & IFN-gamma +ve feedback
Release IFN-gamma
activates NK cells & macrophages & CTLs
IL-2 release → promote T cell proliferation
Th2 cells
induced by IL-4 & IL-13 release from dendritic cells
release IL-4, IL-5, IL-13
IL-4 for further Th2 production
IL-5 for eosinophil recruitment
IL-13 for smooth muscle contraction, epithelial turn over & goblet cell mucus production
induce IgE antibody production
Recruit basophils, eosinophils & M2 macrophage polarisation
Th17 cells
Induced by TGF beta & IL-6
produce IL-17 & IL-22
IL-17 → epithelial cell pro-inflammatory cytokine production
IL-22 → antimicrobial peptide production from epithelial cells & growth + shedding
TFH cells
induced by IL-6 alone
aid B cell activation & class switching
express CD40L to bind to CD40 on B cells to stimulate proliferation
only if activated by binding to peptide fragment expressed on MHC class II
Release IL-21 → B cell activation
Treg cells
tTreg in thymus during development from autoreactive T cells
pTreg in periphery → induced by TGF-beta release
iTreg → made in petri dish
TNF alpha
from macrophages & mast cells
for acute inflammatory response
ICAM expression & P-selectin then E-selectin expression
TGF beta
Treg induction alone
w IL-6 then Th17 induction
Gut= TGF beta high environment → pTreg
released from Treg → cross inhibition of Th1 & Th2
type 1 IFN (alpha & beta etc)
from cells that detect viral infection via PRRs (IRF3/7)
induce antiviral state by binding to jak-STAT signalling then ISGF-3
type II IFN (gamma)
from Th1 for further Th1 induction & cross-inhibition
CXCL8
from macrophages
induce LFA-1 conformational change (bind CXCR1 on neutrophils)
neutrophil activation
sticks to ECM to form gradient for chemotaxis
CD3
on T cells → associates w TCR
has ITAM - immunoreceptor tyrosine based activation motif
phosphorylated
CD20
B cell marker
Rituximab = mAb anti CD20 for B lymphoma & biological DMARD
CD40 & CD40L
For split tolerance
CD40L on TFH
CD40 on B-cell
CD28 & B7 (CD80/86)
B7 on activated dendritic cells
CD28 on T cells binds
T cell licensing
CTLA4
on Treg cells for binding B7 & transendocytosis to remove
abatacept= fusion protein of CTLA4 & Fc of IgG1
Influenza type
-ve sense ssRNA
replication in nucleus using cap snatching (5’cap of host mRNA)
SARS-Cov-2 type
+ve sense ssRNA
w proof readinghe
Hepatitis A
+ve sense ssRNA
Hepatitis B
partial dsDNA genome
reversivirus uses reverse transcription w/o genome integration
Hepatitis C
+ve sense ssRNA
large variability= no vaccine
HIV
+ve ssRNA
retrovirus
Smallpox
dsDNA virus
Pox viruses
dsDNA viruses (but replicate in cytoplasm & have enzymes for transcription of DNA genome & packaging)
Herpes simplex virus
dsDNA virus that can cause latent infections
human cytomegalovirus
dsDNA virus
HPV
200 types -dsDNA virus
HPV 16 & 18 associated with cervical carcinoma
Poliovirus
positive strand ssRNA
poliomyelitis via motor neuron spread
Herpes viruses
Establish latency
dsDNA
enveloped